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Local control of skeletal muscle blood flow during exercise: influence of available oxygen
Journal article   Open access   Peer reviewed

Local control of skeletal muscle blood flow during exercise: influence of available oxygen

Darren P Casey and Michael J Joyner
Journal of applied physiology (1985), Vol.111(6), pp.1527-1538
12/2011
DOI: 10.1152/japplphysiol.00895.2011
PMCID: PMC3233894
PMID: 21885800
url
https://doi.org/10.1152/japplphysiol.00895.2011View
Published (Version of record) Open Access

Abstract

Reductions in oxygen availability (O(2)) by either reduced arterial O(2) content or reduced perfusion pressure can have profound influences on the circulation, including vasodilation in skeletal muscle vascular beds. The purpose of this review is to put into context the present evidence regarding mechanisms responsible for the local control of blood flow during acute systemic hypoxia and/or local hypoperfusion in contracting muscle. The combination of submaximal exercise and hypoxia produces a "compensatory" vasodilation and augmented blood flow in contracting muscles relative to the same level of exercise under normoxic conditions. A similar compensatory vasodilation is observed in response to local reductions in oxygen availability (i.e., hypoperfusion) during normoxic exercise. Available evidence suggests that nitric oxide (NO) contributes to the compensatory dilator response under each of these conditions, whereas adenosine appears to only play a role during hypoperfusion. During systemic hypoxia the NO-mediated component of the compensatory vasodilation is regulated through a β-adrenergic receptor mechanism at low-intensity exercise, while an additional (not yet identified) source of NO is likely to be engaged as exercise intensity increases during hypoxia. Potential candidates for stimulating and/or interacting with NO at higher exercise intensities include prostaglandins and/or ATP. Conversely, prostaglandins do not appear to play a role in the compensatory vasodilation during exercise with hypoperfusion. Taken together, the data for both hypoxia and hypoperfusion suggest NO is important in the compensatory vasodilation seen when oxygen availability is limited. This is important from a basic biological perspective and also has pathophysiological implications for diseases associated with either hypoxia or hypoperfusion.
Reflex - physiology Oxygen - physiology Physical Exertion - physiology Humans Nitric Oxide - physiology Muscle, Skeletal - physiology Animals Sympathetic Nervous System - physiology Hyperemia - physiopathology Muscle Contraction - physiology Hypoxia - physiopathology Blood Pressure - physiology Exercise - physiology Vasodilation - physiology Adenosine Triphosphate - physiology Blood Flow Velocity - physiology Muscle, Skeletal - blood supply

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